title: HIV-1 and HIV-2 dual infection: lack of HIV-2 provirus correlates with low CD4+ lymphocyte counts.
abstract: OBJECTIVE
  We conducted this study to genetically characterize dual infection in individuals demonstrating a dual serological profile.
  
  
  METHODS
  All subjects were first evaluated by immunoblot for antibody reactivity to the major viral antigens for HIV-1 and HIV-2. Sera were judged to be dual-seropositive if they reacted with strong and equal intensity with the envelope antigens of both HIV-1 and HIV-2 and were confirmed with type-specific recombinant env peptides. We used nested polymerase chain reaction (PCR) to amplify proviral gag and env sequence from peripheral blood mononuclear cell (PBMC) DNA from HIV-1- and HIV-2-infected individuals. Positive amplification was detected after Southern blot hybridization.
  
  
  RESULTS
  Plasmid dilution and mixing showed equivalent sensitivity of HIV-1 and HIV-2 primers that was not altered by heterologous target sequences. The DNA PCR showed 100% sensitivity and specificity for detection of monotypic HIV infection. Serologically defined HIV-dual reactives were evaluated by this assay, with 100% detection in female sex workers (21 out of 21), but only 38.5% detection (five out of 13) in hospitalized patients; all being HIV-1 positive only. The lack of HIV-2 proviral signal was significantly correlated with low CD4+ lymphocyte counts (Pvalue = 0.04).
  
  
  CONCLUSIONS
  The results suggest that HIV dual infection may not be a static condition. Levels of HIV-2 may decrease with disease progression or sequester in tissue reservoirs; our results may also suggest that HIV-1 effectively overgrows HIV-2 in the dually exposed host individual.
authors.affiliation: Harvard AIDS Institute, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
authors.forename: A D
authors.initials: AD
authors.lastname: Sarr
authors.forename: D J
authors.initials: DJ
authors.lastname: Hamel
authors.forename: I
authors.initials: I
authors.lastname: Thior
authors.forename: E
authors.initials: E
authors.lastname: Kokkotou
authors.forename: J L
authors.initials: JL
authors.lastname: Sankalé
authors.forename: R G
authors.initials: RG
authors.lastname: Marlink
authors.forename: E M
authors.initials: EM
authors.lastname: Coll-Seck
authors.forename: M E
authors.initials: ME
authors.lastname: Essex
authors.forename: T
authors.initials: T
authors.lastname: Siby
authors.forename: I
authors.initials: I
authors.lastname: NDoye
authors.forename: S
authors.initials: S
authors.lastname: Mboup
authors.forename: P J
authors.initials: PJ
authors.lastname: Kanki
mesh_terms: D015139:Blotting, Southern; D018791:CD4 Lymphocyte Count; D004279:DNA, Viral / Q000097:blood; D018450:Disease Progression; D005260:Female; D015483:HIV Antibodies / Q000097:blood; D015488:HIV Antigens / Q000097:blood; D015658:HIV Infections / Q000175:diagnosis / Q000276:immunology / Q000821:virology*; D015497:HIV-1 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D015498:HIV-2 / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D015151:Immunoblotting; D016133:Polymerase Chain Reaction; D011533:Proviruses / Q000302:isolation & purification*; D012680:Sensitivity and Specificity
chemical_list: D004279:DNA, Viral; D015483:HIV Antibodies; D015488:HIV Antigens